期刊
CELL METABOLISM
卷 34, 期 10, 页码 1486-+出版社
CELL PRESS
DOI: 10.1016/j.cmet.2022.09.007
关键词
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资金
- NIH [R01DK099512, R01HL118601, R01DK102696, R01DK105072, R01HL140574, K99HL148500]
- Spanish Government of Investigation, Development and Innovation [SAF2017-84135-R]
- FEDER
- Autonomous Community of the Region of Murcia through the Seneca Foundation [20795/PI/18]
- NIDDK [R01DK099512]
- Alexander von Humboldt Foundation
- American Diabetes Association [1 -17 -PDF -103]
- [UL1TR001102]
- [UL1TR002541]
- [DK020595]
Late eating is associated with increased risk of obesity, possibly due to increased hunger, altered appetite-regulating hormones, disrupted energy balance, and enhanced adipogenesis.
Late eating has been linked to obesity risk. It is unclear whether this is caused by changes in hunger and appe-tite, energy expenditure, or both, and whether molecular pathways in adipose tissues are involved. Therefore, we conducted a randomized, controlled, crossover trial (ClinicalTrials.gov NCT02298790) to determine the ef-fects of late versus early eating while rigorously controlling for nutrient intake, physical activity, sleep, and light exposure. Late eating increased hunger (p < 0.0001) and altered appetite-regulating hormones, increasing waketime and 24-h ghrelin:leptin ratio (p < 0.0001 and p = 0.006, respectively). Furthermore, late eating decreased waketime energy expenditure (p = 0.002) and 24-h core body temperature (p = 0.019). Adipose tis-sue gene expression analyses showed that late eating altered pathways involved in lipid metabolism, e.g., p38 MAPK signaling, TGF-b signaling, modulation of receptor tyrosine kinases, and autophagy, in a direction consistent with decreased lipolysis/increased adipogenesis. These findings show converging mechanisms by which late eating may result in positive energy balance and increased obesity risk.
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